ESSENTIALS OF DIAGNOSIS
Stage 1 hypertension is defined as an average systolic blood pressure (SBP) of 130 to 139 mm Hg or an average diastolic blood pressure (DBP) of 80 to 89 mm Hg.
Stage 2 hypertension is defined as an average SBP ≥140 mm Hg or DBP ≥90 mm Hg.
Per the 2017 American College of Cardiology/American Heart Association task force, blood pressure (BP) is categorized into four levels based on average SBP and DBP measurements:
Normal (BP <120/80 mm Hg)
Elevated (SBP 120–129 mm Hg and DBP <80 mm Hg)
Stage 1 hypertension (SBP 130–139 mm Hg or DBP 80–89 mm Hg)
Stage 2 hypertension (SBP ≥140 mm Hg or DBP ≥90 mm Hg)
BP measurements should be accurate, and classification should be based on at least two readings obtained on at least two occasions. Individuals with SBP and DBP in different categories should be classified based on the higher category.
Hypertension is very common among older adults and is a major risk factor for cardiovascular (CV) and cerebrovascular morbidity and mortality. In general, SBP rises with age, but DBP rises until about 55 years of age, and then gradually falls thereafter. The prevalence of hypertension is as high as 77% in those 65 to 74 years old and 85% in those ≥75 years old. In 2010, hypertension was the leading cause of death worldwide. Risk factors for hypertension include obesity, reduced physical activity, excess alcohol consumption, lower potassium intake, and excessive salt intake.
Elevated pulse pressure, which is SBP minus DBP, is increasingly being recognized as an important predictor of cerebrovascular and cardiac risk in older adults. Pulse pressure increases with age in a manner parallel to the increase in SBP.
Hypertension in older adults is largely caused by increased arterial stiffness (collagen replacing elastin in the elastic lamina of the aorta) that accompanies aging, but there are other established pathophysiologic mechanisms that contribute to hypertension. Endothelial dysfunction contributes by decreasing availability of vasodilators such as prostacyclin, nitric oxide, and natriuretic peptides. In addition, age-related renal dysfunction causes alterations in the renin-angiotensin-aldosterone system, is associated with glomerulosclerosis and interstitial fibrosis, and is hastened with acute injury or chronic conditions affecting renal function. These changes are associated with increases in oxidative stress in renal and arteriolar vascular tissues. Aside from a resultant reduction in glomerular filtration rate, other homeostatic mechanisms are affected (eg, membrane sodium/potassium adenosine triphosphatase), leading to increased intracellular sodium, reduced sodium-calcium exchange, volume expansion, and resultant hypertension. Reduced renal tubular mass provides fewer transport pathways for potassium excretion, making older hypertensive patients more prone to development of hyperkalemia.
Systemic and renal vascular stiffness secondary to inflammation can be a cause and a consequence of hypertension. Elevated markers for vascular inflammation (eg, C-reactive protein, tumor necrosis ...